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At least 19 recordsLinked to original sources
PubMed1983

Prevention of dextran-induced anaphylactic reactions by hapten inhibition. III. A Scandinavian multicenter study on the effects of 20 ml dextran 1, 15%, administered before dextran 70 or dextran 40.

In an open, prospective multi-center study prevention of dextran-induced anaphylactic reactions (DIAR) was attempted by intravenous injection of 20 ml dextran 1, 15%, Mw 1000 dalton, (Promiten), two minutes before start of infusion of dextran 70 (Macrodex) or dextran 40 (Rheomacrodex). Of 34955 patients investigated, only one developed a severe DIAR of grade III (0.003%). The incidence of severe DIAR after preinjection of 20 ml dextran 1 is significantly lower than that after injection of 10 ml dextran 1 (p = 0.01), and is also markedly lower than that of a large Swedish historical control material (0.037-0.050%). The incidence of mild DIAR is not affected by dextran 1. Adverse reactions to dextran 1 of a generally mild and short-lasting nature were observed in 20 patients. It is recommended that patients who are going to receive dextran 70 or 40 are given a prophylactic i.v. injection of 20 ml dextran 1 before the first unit of clinical dextran to minimize the risk of severe DIAR.

Adolescent↗
PubMed1983

Prevention of dextran-induced anaphylactic reactions by hapten inhibition. II. A comparison of the effects of 20 ml dextran 1, 15%, administered either admixed to or before dextran 70 or dextran 40.

The incidence of dextran-induced anaphylactoid/anaphylactic reactions (DIAR) was investigated after hapten inhibition employing two different modes of administration of dextran 1 (Mw 1 000 dalton). The trial was carried out as an open prospective study that comprised 12 060 patients. They were randomized into two groups--one receiving a mixture of 20 ml dextran 1, 15%, (Promiten) and 500 ml dextran 70 (Macrodex) or dextran 40 (Rheomacrodex) (admixture group), the other receiving an intravenous injection of 20 ml dextran 1, 15% before the infusion of dextran 70 or 40 (preinjection group). DIAR were graded according to severity from I to V. In the admixture group eight DIAR of grade II, one of grade IV and one of grade V were observed, while in the preinjection group two DIAR of grade II occurred. The admixture of dextran 1 to dextran 70 or 40 does not prevent the occurrence of severe DIAR in the dose investigated.

Adolescent↗
PubMed1983

Prevention of dextran-induced anaphylactic reactions by hapten inhibition. I. A Scandinavian multicenter study on the effects of 10 ml dextran 1, 15% administered before dextran 70 or dextran 40.

In an open prospective study the prevention of dextran-induced anaphylactic reactions (DIAR) by hapten inhibition was investigated in 29 252 patients. Forty-nine hospitals in Sweden, Norway and Finland participated in the study which was running for two years. Ten ml of dextran 1, 15%, (Promiten, Pharmacia AB, Uppsala, Sweden) with a weight average molecular weight of 1 000 dalton was injected intravenously two minutes before infusion of dextran 70 (Macrodex) or dextran 40 (Rheomacrodex). DIAR were graded according to severity from I to V. Six grade III and one grade IV reactions occurred, representing an incidence of severe DIAR of 0.024%. Compared to a large historical control material, preinjection of 10 ml of dextran 1 exerts a partially protective effect, but no statistical proof can be given. Consequently trials have been started with a 20 ml dose of dextran 1. Adverse reactions to the preinjection of 10 ml of dextran 1 were observed in 0.072%. These reactions were of a mild and shortlasting nature and considered to be of minor clinical importance.

Adolescent↗
PubMed1974

Influence of DEAE-dextran, polybrene, dextran and dextran sulphate on spontaneous leukaemia development in AKR mice and virus induced leukaemia in BALB-c mice.

AKR mice of which more than 90% die of lymphatic thymus leukaemia, had their mean survival time increased by weekly intraperitoneal inoculation of either of the two polycations DEAE-dextran and polybrene. Administration of the neutral dextran had no effect, whereas the polyanion dextran sulphate accelerated leukaemia development.Adult BALB/c mice infected with Rauscher leukaemia virus and treated from the time of palpable spleen enlargement, showed a life prolonging effect of the polycations DEAE/dextran and polybrene, and of neutral dextran. BALB/c mice treated from the time of leukaemia infection, however, showed a life prolonging effect with polyanion dextran sulphate and also of neutral dextran.

Animals↗
PubMed1980

[Hapten inhibition: inhibition of antibody dependent dextran side effects by means of low molecular dextran (dextran 1) as a monovalent hapten].

Dextran-induced anaphylactoid reactions can be attributed to preformed circulating antibodies cross-reacting with dextrans. Therefore, after intravenous administration of clinical dextran, formation of immune complexes with resulting complement activation and secondary formation and/or release of mediators with clinical symptoms of an immune complex or aggregate anaphylaxis can occur (type-III immune reaction). Antigen antibody reactions can be prevented if the antigen-binding sites of the antibodies are specifically blocked by monovalent haptens (low molecular non-immunogenic antigens). The effectiveness of this principle of 'hapten inhibition' could be proven in vitro as well as in animal experiments. In volunteer studies intravenous administration of the low molecular dextran in a 15% solution (Dextran 1), with a molecular weight around 1,000 functioning as monovalent hapten, was well tolerated.

Anaphylaxis↗
PubMed1981

Immunochemical studies on dextrans. Cross-reaction of synthetic linear dextrans with rabbit anti-N4 dextran.

Alpha (1 Leads to 6) specific anti-dextran antibody was raised in rabbits by injecting N4 dextran-concanavalin A conjugate, and the interactions of five synthetic linear dextrans (alpha(1 Leads to 6)-D-glucopyranans) with rabbit anti-N4 dextran were studied. The ability of glucans to precipitate antibody depended on their average molecular weight, samples with higher molecular weight precipitating more antibody nitrogen under the same conditions. This phenomenon was shown to be due to solubility of the antigen-antibody complex. Oligosaccharide inhibition assay indicated that the maximum size of the alpha(1 Leads to 6)-specific antibody combining site corresponded to isomaltopentaose. The precipitated antibody class was shown to be IgG immunoglobulin, and it was mostly directed to linear non-terminal glucosidic linkages. Determination of antibody nitrogen and glucan in the precipitates indicated that the ratio of antibody molecule to numbers of glucose residues was 1:16 in the extreme antibody excess region.

Animals↗
PubMed2001

Transience in polyion complexation between nicotinamide-modified dextran and carboxymethyl dextran during enzymatic degradation of dextran.

A self-regulated degradation system using polyion complexation through oxidation reaction from degradation products was preliminarily studied. 1,4-Dihydronicotinamide-modified dextran (NAH-Dex) with different molecular weights was prepared, and NAH moiety in NAH-Dex was oxidized by H2O2 to the dehydrated form (NA+-Dex). The dependence of stoichiometry, concentration, and molecular weight on polyion complexation with carboxymethyl dextran (CMD) were examined. NA+-Dex with a molecular weight above 40000 formed an insoluble complex with CMD, and the complexation was found to proceed stoichiometrically. The extent of polyion complexation was dependent on the concentration of NA+-Dex and CMD, whereas the time to reach complexation was dependent on H2O2 concentration. When H2O2 and dextranase were added to the solution containing NAH-Dex, CMD, and dextran, transmittance dropped and then increased again. From these results, the addition of dextran into the system of H2O2, NAH-Dex, CMD, and dextranase can regulate formation and dissociation of the polyion complex between NA+-Dex and CMD. The antagonistical inhibition of the degradation of the polyion complex is a key parameter of the self-regulated degradation system.

Biocompatible Materials↗
PubMed2003

Sodium ferric gluconate complex in hemodialysis patients. II. Adverse reactions in iron dextran-sensitive and dextran-tolerant patients.

BACKGROUND: Iron dextran administration is associated with a high incidence of adverse reactions including anaphylaxis and death. Although dextran, rather than iron, is believed to be the cause of these reactions, it is not known whether iron dextran-sensitive patients can be safely administered another form of parenteral iron, sodium ferric gluconate in sucrose (SFGC). METHODS: In a 69 center, prospective, double-blind, controlled trial of safety and tolerability of SFGC, the rate of reactions to SFGC and placebo in 144 iron dextran-sensitive patients was compared with 2194 patients who were previously tolerant to iron dextran preparations. Serum tryptase levels, a marker of mast cell degranulation, also were measured. RESULTS: Among 143 iron dextran-sensitive patients exposed to SFGC, three (2.1%) were intolerant. All three had suspected allergic events to SFGC, including one patient with a serious reaction (0.7%). One dextran-sensitive patient (0.7%) had a suspected allergic reaction after placebo. In contrast, among 2194 iron dextran-tolerant patients, reactions to SFGC were significantly less common, with SFGC intolerance seen in seven patients (0.3%; P = 0.020), including five (0.2%) who had suspected allergic events (P = 0.010), but none who had serious events (0.0%; P = 0.061). Two iron dextran-tolerant patients (0.09%) had allergic-like reactions following placebo injections. Two of the three suspected allergic events in the iron dextran-sensitive group were confirmed as mast cell dependent by a 100% increase in serum tryptase, while there were no confirmed allergic events in the iron dextran-tolerant group. Long-term exposure to SFGC in iron dextran-sensitive patients resulted in intolerance in only one additional patient and no serious adverse events. CONCLUSIONS: Patients with a history of iron dextran sensitivity had approximately sevenfold higher rates of reaction to both placebo and SFGC compared to iron dextran tolerant patients. However, logistic regression analysis, performed to account for the higher reaction rate to placebo, suggests that this increased reactivity was not drug-specific nor immunologically mediated, but represented host idiosyncrasy. These results support the conclusions that reactions to SFGC can be attributed to pseudoallergy, and that SFGC is not a true allergen.

Drug Hypersensitivity↗
PubMed1983

Inhibition by low molecular weight dextran of the blood pressure fall and the lowering of plasminogen proactivator induced by clinical dextran in the rat.

The intravenous injection into rats of dextran with a molecular weight of 1,000 (LMr dextran) in doses greater than or equal to 200 mg/kg induced rapid, but transient falls in blood pressure. Pretreatment of the rats with LMr dextran 200 mg/kg caused a partial inhibition of the profound blood pressure fall induced by the injection of clinical dextran with a molecular weight of 70,000 (HMr dextran), 40 mg/kg. In accordance with previous works (Briseid & Berstad 1981; Berstad & Briseid 1982; Berstad 1982) it was found that the intravenous injection of HMr dextran lowered the plasma levels of plasminogen proactivator (pro-PGA) and functionally active high molecular weight kininogen (HMrK). Also LMr dextran, 200 mg/kg, induced significant reductions in the mentioned parameters, but less extensive than those obtained by HMr dextran, 40 mg/kg, and pretreatment of the rats with LMr dextran inhibited the subsequent effects of HMr dextran. It is suggested that a dextran-activated plasminogen activator might be an early link in the mechanism underlying the dextran-induced state of shock in the rat.

Animals↗
PubMed1985

Isotypes of antibodies induced by plain dextran or a dextran-protein conjugate.

Mice were immunized with alpha (1----6) dextran or its protein conjugate with monthly intervals, and their antibodies were quantitated with an isotype-resolved radioimmunoassay. Plain dextran (molecular weight = 5-40 million) induced antibody concentrations varying from 20 to 80 micrograms/ml (primary response). The response to a booster injection was weaker than the response to the first injection. More than 90% of anti-dextran antibodies were IgM but IgG and IgA responses could be unequivocally demonstrated. IgG1 and IgG3 were the predominant subclasses of IgG. Dextran antibody responses to a conjugate of dextran (molecular weight approximately equal to 10000) and chicken serum albumin (CSA) were stronger (80-300 micrograms/ml) than responses to plain dextran, and anti-CSA responses to the conjugate were even stronger (up to 900 micrograms/ml). Three distinctly different isotype patterns were observed. A pattern IgM much greater than IgG1 = IgG3 greater than IgG2a prevailed in responses to the plain dextran and in primary anti-dextran responses to dextran-CSA. Another pattern IgG1 greater than IgG3 greater than IgM greater than IgG2a was observed in late anti-dextran responses to dextran-CSA. The third pattern IgG1 much greater than IgG2a greater than IgG3 approximately equal to IgM was characteristic of anti-CSA antibodies. Little IgG2b or IgA antibodies were found. Different isotype patterns can best be explained on the basis of secondary factors such as T cell help.

Animals↗
PubMed1995

Biliary secretion of antibody to dextran following oral immunization with dextran B512.

Anti-dextran in bile was induced to high levels by oral immunization with dextran B512. IgM anti-dextran were dominant in serum, whereas IgG anti-dextran was dominant in bile. The binding properties of these IgM and IgG antibodies were different, as determined by ELISA with several dextrans. Splenocytes produced equal amounts of IgG and IgM antidextran but cells from mesenteric lymph nodes (MLN) and Peyer's patches produced mainly IgG anti-dextran. Differences were observed among different strains of mice in their ability to produce anti-dextran in serum and bile upon immunization with dextran. BALB/c mice, which are intermediate responders in terms of their serum antibody levels, produced high levels of anti-dextran in bile. C3H/He and C57BL/6, which are high responders in terms of serum antibody levels, had intermediate responses in bile. DBA/2, which are low responders in terms of serum antibody levels, showed low responses in bile. The results provide further evidence of the existence of anti-dextran producing cells. These results indicate that B cells in systemic and mucosal-associated lymphoid tissues from BALB/c, C3H/He, C57BL/6 and DBA/2 mice respond differently to oral immunization with dextran B512.

Administration, Oral↗
PubMed1993

Hapten inhibition of dextran anaphylaxis. Nine years of post-marketing surveillance of dextran 1.

All spontaneous reports to the manufacturer and to WHO's database INTDIS regarding adverse reactions to clinical dextran after preinjection of dextran 1 and to dextran 1 alone 1983-1991 were collected. During 1983-1991 a total of 4.8 million doses of Promit were sold in fourteen countries. The incidence of severe DIAR (grades III-V) to clinical dextran after the prophylactic use of hapten inhibition was approximately one case per 200,000 doses of dextran 1. In Sweden, where reporting of severe adverse drug reactions is mandatory, the incidence was one case per 70,000. This indicates a 35-fold reduction in the incidence of severe DIAR compared with the use of clinical dextran without dextran 1. Only two fatal reactions were reported; the incidence was therefore one case per 2.4 million doses, indicating a 77-fold reduction. Both these occurred in patients with extremely high titers of DRA. Side effects to dextran 1, mostly mild, were reported in one case per 100,000 doses. These side effects were not antibody mediated. It is concluded that the introduction of hapten inhibition with dextran 1 has greatly reduced the risk for serious side effects to dextran, making dextran one of the safest colloids in use.

Anaphylaxis↗
PubMed1987

Role of dextran-specific suppressor T cells in the regulation of the immune response by a reactive form of dextran.

Reactive forms of antigens or haptens have been shown to induce a state of hyporesponsiveness mediated in part by suppressor T cells. Injection of Balb/c x C57B16 F1 (CB6F1) mice with a reactive form of dextran B1355S (periodate oxidized dextran, dex-P) specifically reduced responses to dextran immunization within 1 day after dex-P treatment. This unresponsiveness lasted at least 23 days and required a reactive form of dextran for its induction since native dextran and oxidized/reduced dextran failed to induce tolerance. Furthermore, hyporesponsiveness could be induced by iv injection of dextran-coupled cells, especially peripheral blood lymphocytes, a result which suggests that in vivo coupling to cellular antigens is involved in dex-P-induced hyporesponsiveness. Suppression of the anti-dextran response could be transferred to normal mice with T-cell-enriched spleen cell populations from dex-P-injected mice. Interestingly, the presence of B cells in the transferred cell preparations interfered with detection of suppression. Both Lyt 1+2- and Lyt 1-2+ cells were involved in the dex-P-induced suppression; indeed, mixtures of these types of T cells led to the most profound degree of suppression. The suppressive activity of spleen cells from dex-P-injected mice could be removed by passage over dextran-coated plates. Moreover, cells eluted from the plates specifically suppressed anti-dextran responses of normal mice, indicating that dex-P injection induces a population of antigen-binding suppressor cells. This system will allow the study of the suppressor-T-cell receptors in a well-defined idiotypic system.

Animals↗
PubMed1987

Regulation of the anti-alpha (1,3) dextran response: two populations of dextran-reactive B cells that differ in their T cell requirements for induction to antibody synthesis.

The in vitro antibody response to dextran B1355S, a thymus-independent Type 2 antigen, requires T cell-derived lymphokines but is not thought to require an activation signal from an antigen-specific T helper cell. The present study demonstrates that there are two dextran-reactive B cell populations in BALB/c mice with respect to the T cell requirements for the generation of antibody-forming cells. One population found among dextran-reactive spleen B cells from 12- to 14-mo-old BALB/c mice generated anti-dextran PFC in the presence of B cell growth factor (BCGF II) and IL 2 or the combination of BCGF II, IL 2, and IFN-gamma. A second population of dextran-reactive B cells found in spleen and Peyer's patches of 2-mo-old unprimed mice did not respond to these same lymphokines, but did generate anti-dextran plaque-forming cells in the presence of Thy-1.2+, L3T4+ T cells from Peyer's patches. However, splenic B cells obtained from 2-mo-old mice that had been primed with dextran 2 to 3 days after birth were shown to be responsive to the same lymphokines as dextran-reactive B cells from 12- to 14-mo-old mice. These results suggest that previous priming with dextran B1355S induces a dextran-specific B cell population that can be activated to antibody-forming cells in the presence of antigen and T cell-derived lymphokines, whereas a second, unprimed population requires an additional activation signal from L3T4+ T cells.

Animals↗
PubMed1994

Size-dependent separation of proteins in the presence of sodium dodecyl sulfate and dextran in capillary electrophoresis: effect of molecular weight of dextran.

Dextran solutions are widely used as sieving medium in protein analysis by capillary electrophoresis in the presence of sodium dodecyl sulfate. We studied the effect of dextran molecular weight on the separation efficiency using different dextran preparations with wide and very narrow molecular weight distributions, in the range between 1270 and 2,000,000. Migration times and band broadening of proteins were significantly affected by the molecular weight of dextran. Migration times of proteins decreased as molecular weights of the dextrans decreased. Satisfactory separation of all the proteins was possible with all dextrans except those with molecular weights of 70,000 and 23,800 where bovine serum albumin and phosphorylase b failed to be separated. Unexpectedly rapid separation of all the proteins with enhanced resolution could be observed using two dextrans with a narrow molecular weight distribution, with molecular weights of 1270 and 5220. Clearly the use of dextran with higher molecular weight is not the only way to achieve efficient separation of proteins. The separation mechanism in the presence of the low molecular weight dextrans remains to be made clear in a future study.

Carbonic Anhydrases↗
PubMed1982

Histamine release induced by dextran: the nature of the dextran receptor.

Dextrans of molecular weight 10(4) to 2 x 10(6) induced histamine release from rat peritoneal mast cells in the presence of calcium (1 mM) and phosphatidyl serine (10 micrograms/ml). Glucose and low molecular weight dextrans inhibited the histamine release induced by high molecular weight dextrans but the inhibition could not be explained in terms of a simple competitive model. Structure-activity relationships for the inhibition of dextran-induced histamine release by a number of saccharides demonstrated that substitution at the C-3, C-4, and C-6 positions of glucose were most important for activity. Inhibition of histamine release by glucose was specific for the dextran stimulus. Soluble IgE and IgG antibodies failed to interfere with histamine release induced by dextran. Phlorizin specifically inhibited the histamine release induced by dextran. Purification of mast cells on albumin or ficoll gradients produced a selective loss of response to dextran which was not due to the removal of non-mast cells but to some change in the mast cells themselves. The possible nature of the dextran receptor is discussed.

Animals↗